| First Author | Nakazawa T | Year | 2006 |
| Journal | EMBO J | Volume | 25 |
| Issue | 12 | Pages | 2867-77 |
| PubMed ID | 16710293 | Mgi Jnum | J:119025 |
| Mgi Id | MGI:3701026 | Doi | 10.1038/sj.emboj.7601156 |
| Citation | Nakazawa T, et al. (2006) NR2B tyrosine phosphorylation modulates fear learning as well as amygdaloid synaptic plasticity. EMBO J 25(12):2867-77 |
| abstractText | Phosphorylation of neural proteins in response to a diverse array of external stimuli is one of the main mechanisms underlying dynamic changes in neural circuitry. The NR2B subunit of the NMDA receptor is tyrosine-phosphorylated in the brain, with Tyr-1472 its major phosphorylation site. Here, we generate mice with a knockin mutation of the Tyr-1472 site to phenylalanine (Y1472F) and show that Tyr-1472 phosphorylation is essential for fear learning and amygdaloid synaptic plasticity. The knockin mice show impaired fear-related learning and reduced amygdaloid long-term potentiation. NMDA receptor-mediated CaMKII signaling is impaired in YF/YF mice. Electron microscopic analyses reveal that the Y1472F mutant of the NR2B subunit shows improper localization at synapses in the amygdala. We thus identify Tyr-1472 phosphorylation as a key mediator of fear learning and amygdaloid synaptic plasticity. |
